The purpose of this research is to develop a model for the induction of choriocarcinoma from normal rat trophectoderm. The inductive procedure consists of fetectomy, prolongation of the luteal phase, and administration of a carcinogenic drug. Fetectomy arrests the normal differentiation of the placenta. If fetectomy is carried out before gestation day 12, the placenta persists composed almost entirely of basal zone trophectoderm in which the percentage of trophoblast giant cells is also increased. Choriocarcinoma can be induced on this substratum by carcinogenic drugs. The time necessary for induction is gained by prolongation of the luteal phase with administered progesterone. Progression of normal to malignant cells will be monitored by studies of the endocrine function of the persisting trophectoderm, the ontogeny of hormone receptors, and aberrations in the interactions of the trophectoderm with uterine cells, in vivo and as monolayers, in vitro. Any tumors developed will be used in an attempt to culture a cell line from rat choriocarcinoma which can be characterized and used for in vitro studies. The correlation of these data will provide facts which may help explain the control of the trophectoderm through the essential but potentially destructive invasive processes of normal implantation and the mechanisms which have failed when choriocarcinoma develops.